USP10 通过稳定 SIRT6 拮抗 c-Myc 转录激活,从而抑制肿瘤形成。

USP10 antagonizes c-Myc transcriptional activation through SIRT6 stabilization to suppress tumor formation.

机构信息

Department of Pathology, Northwestern University Feinberg School of Medicine, 303 East Chicago Avenue, Chicago, IL 60611, USA.

Department of Pathology, Northwestern University Feinberg School of Medicine, 303 East Chicago Avenue, Chicago, IL 60611, USA.

出版信息

Cell Rep. 2013 Dec 26;5(6):1639-49. doi: 10.1016/j.celrep.2013.11.029. Epub 2013 Dec 12.

Abstract

The reduced protein expression of SIRT6 tumor suppressor is involved in tumorigenesis. The molecular mechanisms underlying SIRT6 protein downregulation in human cancers remain unknown. Using a proteomic approach, we have identified the ubiquitin-specific peptidase USP10, another tumor suppressor, as one of the SIRT6-interacting proteins. USP10 suppresses SIRT6 ubiquitination to protect SIRT6 from proteasomal degradation. USP10 antagonizes the transcriptional activity of the c-Myc oncogene through SIRT6, as well as p53, to inhibit cell-cycle progression, cancer cell growth, and tumor formation. To support this conclusion, we detected significant reductions in both USP10 and SIRT6 protein expression in human colon cancers. Our study discovered crosstalk between two tumor-suppressive genes in regulating cell-cycle progression and proliferation and showed that dysregulated USP10 function promotes tumorigenesis through SIRT6 degradation.

摘要

SIRT6 肿瘤抑制因子的蛋白表达减少与肿瘤发生有关。SIRT6 蛋白在人类癌症中下调的分子机制尚不清楚。我们使用蛋白质组学方法鉴定了泛素特异性肽酶 USP10(另一种肿瘤抑制因子)是 SIRT6 的相互作用蛋白之一。USP10 抑制 SIRT6 的泛素化,以保护 SIRT6 免受蛋白酶体降解。USP10 通过 SIRT6 以及 p53 拮抗 c-Myc 癌基因的转录活性,从而抑制细胞周期进程、癌细胞生长和肿瘤形成。为了支持这一结论,我们检测到人类结肠癌中 USP10 和 SIRT6 蛋白表达均显著降低。我们的研究发现,两个肿瘤抑制基因之间存在相互作用,调节细胞周期进程和增殖,并且表明失调的 USP10 功能通过 SIRT6 降解促进肿瘤发生。

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